[unreadable] HSV-1 is responsible for the majority of blinding corneal infections in industrialized countries due to recurrences. Repeated recurrences can lead to irreversible corneal scarring. HSV establishes latency in neurons in the trigeminal ganglia (TG). The molecular mechanism(s) underlying viral neural reactivation are not known. Histone acetylation and deacetylation have been shown to play important roles in transcriptional regulation and recent evidence has shown that specific histone tail modification acts as a determinant for HSV-1 gene expression of one important viral transcript. To explore one epigenetic factor, histone acetylation, involved in gene regulation of the HSV-1 genome, further studies are needed. These studies will employ the use of HSV-1 strains that are high and low in vivo phenotypic reactivators to compare the histone acetylation in relation to viral gene regulation during the transition from latency to reactivation. Using the mouse eye model, my specific goals are to determine the acetyl H3 association of four viral genes (DNA) in the mouse TG in latency and induced reactivation, using the HSV-1 strains 17Syn+ (high phenotypic reactivator) and F (low phenotypic reactivator). [unreadable] [unreadable]